Cerebral cortex
Cerebral cortex: lobes, Brodmann areas, speech areas and aphasias
Cerebral cortex for FCPS Part 1: Brodmann areas, cortical layers, the homunculus, aphasia types and lobe syndromes. Explains macular sparing, paracentral lesions, cortical deafness, akinetic mutism and colour blindness from V4 damage.
One of the most tested topics in past papers
Functional areas
| Area | Location (Brodmann) | Effect of a lesion |
|---|---|---|
| Primary motor | Precentral gyrus (4) | Contralateral UMN weakness |
| Premotor and supplementary motor | 6 | Apraxia; poor planning and initiation of movement |
| Frontal eye field | 8 | Eyes deviate towards a destructive lesion |
| Broca's area | Inferior frontal gyrus, dominant side (44, 45) | Expressive aphasia |
| Prefrontal cortex | 9–12, 46 | Personality change, disinhibition, poor judgement, apathy |
| Primary somatosensory | Postcentral gyrus (3, 1, 2) | Contralateral loss of touch and position sense |
| Sensory association | Superior parietal lobule (5, 7) | Astereognosis, sensory inattention |
| Primary auditory | Transverse temporal (Heschl's) gyri (41, 42) | Little deafness if one side only |
| Wernicke's area | Posterior superior temporal gyrus, dominant (22) | Receptive aphasia |
| Angular gyrus | Dominant inferior parietal (39) | Alexia with agraphia, anomia, Gerstmann |
| Supramarginal gyrus | 40 | Conduction aphasia, apraxia |
| Primary visual | Banks of calcarine sulcus (17) | Contralateral homonymous hemianopia |
| Gustatory | Parietal operculum and insula (43) | Loss of taste |
| Colour area (V4) | Ventral occipitotemporal (fusiform, lingual) cortex | Achromatopsia |
| Face area | Fusiform gyrus | Prosopagnosia |
Cortical layers
| Layer | Name | Main role |
|---|---|---|
| I | Molecular | Mostly dendrites and axons |
| II | External granular | Cortico-cortical connections |
| III | External pyramidal | Association and commissural output |
| IV | Internal granular | Receives thalamic input; thick in sensory cortex |
| V | Internal pyramidal | Output to brainstem and cord; contains Betz cells in area 4 |
| VI | Multiform | Output to thalamus |
- Sensory cortex (areas 3, 17, 41) is "granular" with a thick layer IV; motor cortex is "agranular" with a thick layer V. Betz cells are only a small fraction of corticospinal fibres; they degenerate in motor neurone disease.
Homunculus and the arterial map
- On the motor and sensory strips the face and hand lie on the lateral surface (MCA territory), the leg and foot on the medial surface in the paracentral lobule (ACA territory). The hand, lips and tongue have the largest representation; the trunk has the least.
- So an MCA stroke weakens face and arm more than leg; an ACA stroke weakens the leg.
- The paracentral lobule also controls voluntary bladder function. A parasagittal falx meningioma at the vertex compresses both paracentral lobules, giving slowly progressive spastic weakness of both legs with urinary incontinence and normal arms, which mimics a cord lesion.
- Macular sparing in a PCA infarct: the occipital pole, where the macula is represented, receives collateral supply from the MCA, so central vision survives a PCA occlusion. Macular sparing therefore points to a cortical rather than a tract lesion.
- Each cochlear nucleus projects to both sides, so removing one auditory cortex leaves hearing almost normal; bilateral temporal lesions cause cortical deafness.
Aphasias
| Type | Fluency | Comprehension | Repetition | Lesion |
|---|---|---|---|---|
| Broca's (expressive) | Non-fluent, telegraphic | Good | Poor | Inferior frontal gyrus |
| Wernicke's (receptive) | Fluent, empty jargon | Poor | Poor | Posterior superior temporal gyrus |
| Conduction | Fluent | Good | Poor | Arcuate fasciculus, supramarginal gyrus |
| Global | Non-fluent | Poor | Poor | Large dominant MCA infarct |
| Transcortical motor | Non-fluent | Good | Preserved | Around Broca's area (ACA–MCA watershed) |
| Transcortical sensory | Fluent | Poor | Preserved | Around Wernicke's area |
| Anomic | Fluent | Good | Good | Angular gyrus or temporal lobe |
- Every aphasia includes word-finding difficulty; call it anomic aphasia only when fluency, comprehension and repetition are all normal and naming alone fails.
- A right-handed man with sudden right face and arm weakness who can neither speak fluently nor understand has a left MCA occlusion (global aphasia).
- Dysarthria is a disorder of articulation, not language: comprehension, naming, repetition and writing are normal.
- Language lies in the left hemisphere in about 95% of right-handed and about 70% of left-handed people.
Lobe syndromes
- Frontal: personality change, disinhibition or apathy, poor planning, primitive reflexes (grasp, pout), urinary incontinence, gait apraxia, expressive aphasia if dominant. Anosmia with an olfactory groove meningioma.
- Medial frontal and anterior cingulate: bilateral damage (both ACAs, as after anterior communicating artery aneurysm rupture and vasospasm) causes akinetic mutism: the patient is awake and follows with the eyes but makes no spontaneous speech or movement, despite intact power. Testing power distinguishes it from locked-in syndrome.
- Dominant parietal: Gerstmann syndrome (acalculia, agraphia, finger agnosia, left–right confusion); ideomotor apraxia.
- Non-dominant parietal: hemispatial neglect, anosognosia, dressing and constructional apraxia.
- Either parietal: astereognosis, two-point discrimination loss, sensory inattention, inferior quadrantanopia.
- Temporal: receptive aphasia (dominant), memory loss (hippocampus), superior quadrantanopia (Meyer's loop), déjà vu and olfactory or gustatory hallucinations in temporal lobe epilepsy, Klüver–Bucy syndrome (bilateral amygdala). Herpes simplex encephalitis targets the temporal lobes (fever, confusion, seizures, haemorrhagic oedema); intravenous aciclovir is started at once.
- Occipital: homonymous hemianopia with macular sparing; bilateral lesions cause cortical blindness, sometimes with Anton syndrome (denial of blindness). Bilateral ventral lesions involving V4 cause cerebral achromatopsia: the world appears grey despite normal acuity.
| Feature | Dominant (left) parietal | Non-dominant (right) parietal |
|---|---|---|
| Classic syndrome | Gerstmann | Neglect |
| Apraxia | Ideomotor | Dressing, constructional |
| Insight | Usually preserved | Anosognosia |
Connections and reflexes
- Corpus callosum joins the hemispheres: after section, an object felt by the left hand cannot be named (the information reaches only the non-language right hemisphere).
- Arcuate fasciculus links Wernicke's and Broca's areas.
- Most righting reflexes are integrated in the midbrain; optical righting reflexes need the visual cortex and keep the head upright using vision.
Remember Face and arm are lateral (MCA), leg is medial (ACA); repetition fails only when the perisylvian circuit itself is broken.
Exam trap Macular sparing means a cortical (occipital) lesion with MCA collateral supply, not an optic tract lesion.
Exam trap Bilateral leg UMN weakness with incontinence may come from a falx meningioma, not the spinal cord.
How FCPS asks about this
- Fluent speech, good comprehension, poor repetition: conduction aphasia, arcuate fasciculus.
- Only naming lost after left temporal injury: anomic aphasia.
- Betz cells lie in: layer V (internal pyramidal) of area 4.
- Unilateral auditory cortex removal without deafness: each ear projects to both cortices.
- Awake, mute, motionless after bilateral ACA vasospasm: anterior cingulate damage, akinetic mutism.
- World in shades of grey after bilateral PCA infarcts: V4 in ventral occipitotemporal cortex.
- Neglect of the left side: right (non-dominant) parietal lobe.
Test yourself on this topic
5 of the 73 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
After surgery for intractable drop attacks, a right-handed man, with eyes closed, cannot name a key placed in his left hand, but can pick it out from other objects with the same hand. Objects in his right hand are named normally. Which of the following best explains this?
Answer: Right hemisphere cannot reach left speech areas
Corpus callosotomy is used for drop attacks in some epilepsy syndromes. Touch from the left hand reaches the right somatosensory cortex, which can recognise the object, so the left hand can select it. Naming requires language areas in the left hemisphere, and without the corpus callosum the information cannot cross to them. Right-hand objects reach the left hemisphere directly and are named normally.
Split brain
- Left-hand touch to right hemisphere
- Speech in left hemisphere
- Callosum cut: cannot name left-hand objects
- Can still select by touch
Remember Knows it but cannot name it: disconnection, not sensory loss.
Exam trap Astereognosis from a parietal lesion would stop him selecting the object at all.
Why the other options are wrong
- Right parietal cortex has been damaged He can still identify the object by touch, so parietal function is intact.
- Left hand touch fibres are cut in the cord He can recognise the object, so sensation is intact.
- Left hemisphere cannot reach the left hand Each hemisphere controls the opposite hand; the issue is naming.
- Wernicke's area has been removed Right-hand naming is normal, so language is intact.
A patient speaks fluently and understands well but cannot repeat a sentence spoken to him. Which pathway is damaged?
Answer: Arcuate fasciculus
Conduction aphasia results from damage to the arcuate fasciculus (often supramarginal gyrus region) linking Wernicke's area to Broca's area. Comprehension and spontaneous fluent speech are relatively preserved, but repetition is poor and paraphasic errors occur. In transcortical aphasias, repetition is preserved because the perisylvian loop is intact. Corpus callosum lesions cause disconnection syndromes (e.g. inability to name objects placed in the left hand).
Conduction aphasia
- Lesion: arcuate fasciculus
- Fluent speech, good comprehension
- Poor repetition
- Transcortical aphasias: repetition preserved
Remember Cut the cable, you cannot repeat.
Why the other options are wrong
- Corpus callosum Interhemispheric disconnection.
- Optic radiation Visual field defects.
- Internal capsule Motor and sensory deficits.
- Corticospinal tract Weakness.
After bilateral posterior cerebral artery infarcts, a woman with normal acuity says the world looks only in shades of grey. Which area is damaged?
Answer: Ventral occipitotemporal cortex (V4)
Colour perception depends on the colour-selective area V4 in the ventral occipitotemporal cortex (lingual and fusiform gyri), part of the ventral 'what' stream. Bilateral damage, typically from posterior cerebral artery infarcts, causes cerebral achromatopsia: loss of colour vision with preserved acuity. A unilateral lesion causes loss of colour in the opposite half-field. Lesions of the primary visual cortex or optic radiations cause field defects instead.
Cerebral achromatopsia
- Colour area V4: lingual and fusiform gyri
- Bilateral PCA infarcts: grey world
- Acuity preserved
- Ventral stream = what
Remember A grey world with sharp vision: ventral occipital V4.
Exam trap Optic neuritis also reduces colour vision but with reduced acuity and a central scotoma.
Why the other options are wrong
- Primary visual cortex above calcarine Damage here causes a field defect, not loss of colour.
- Lateral geniculate bodies Would cause field defects.
- Optic radiations in the parietal lobe Would cause an inferior quadrantanopia.
- Superior colliculi Involved in eye movements and visual reflexes, not colour.
Removal of a left temporal tumour with the transverse temporal gyri leaves hearing almost normal. Why is deafness absent?
Answer: Each ear projects to both auditory cortices
The primary auditory cortex lies in the transverse temporal (Heschl) gyri, Brodmann areas 41 and 42. From the cochlear nuclei, fibres ascend on both sides through the superior olivary complex, lateral lemniscus, inferior colliculus and medial geniculate body, so each ear is represented in both hemispheres. A unilateral cortical lesion therefore causes no clear deafness, though sound localisation on the opposite side may be impaired.
Auditory cortex
- Heschl gyri, areas 41, 42
- Each ear goes to both cortices
- One-sided lesion: no deafness
- Unilateral deafness: ear, VIII or cochlear nucleus
Remember One-sided deafness means a lesion below the superior olive.
Exam trap Bilateral temporal lesions can cause cortical deafness.
Why the other options are wrong
- Hearing is processed in the inferior colliculus It is a relay; conscious hearing needs the cortex.
- The right ear projects only to the right cortex Each ear projects bilaterally, mainly contralaterally.
- Wernicke's area takes over hearing Wernicke's area interprets language; it is not the primary auditory area.
- Cochlear nuclei project straight to the thalamus They relay through brainstem nuclei before the thalamus.
A right-handed man has sudden right face and arm weakness (leg less affected) and cannot speak fluently or understand speech. Which artery is blocked?
Answer: Left middle cerebral artery
The middle cerebral artery supplies the lateral surface of the hemisphere, including the motor and sensory areas for the face and arm, and Broca's and Wernicke's areas in the dominant (usually left) hemisphere. A left MCA stroke causes right face and arm weakness and sensory loss more than the leg, aphasia and often a right homonymous hemianopia. Non-dominant MCA strokes cause neglect.
MCA stroke
- Face and arm > leg
- Dominant: aphasia
- Non-dominant: neglect
- Often homonymous hemianopia
Remember MCA: face, arm and language.
Exam trap Global aphasia with both expressive and receptive loss points to a large dominant MCA stroke.
Why the other options are wrong
- Right middle cerebral artery Would cause left-sided signs and neglect.
- Left anterior cerebral artery Leg more than arm.
- Left posterior cerebral artery Visual field loss without major weakness.
- Basilar artery Brainstem signs, often bilateral.
Where this sits in the CPSP syllabus
- Paper 1: Neuroanatomy, Cerebral cortex: lobes, functional areas, speech areas
- Surgery & Allied, Paper 2: Cranium and brain, Cerebral cortex: lobes, functional areas, speech areas
- Medicine & Allied, Paper 2: Central nervous system, Cerebral cortex: lobes, functional areas, speech areas
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